The Tomato Homolog of CORONATINE-INSENSITIVE1 Is Required for the Maternal Control of Seed Maturation, Jasmonate-Signaled Defense Responses, and Glandular Trichome Development[W]
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- Lei Li
- Department of Energy–Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824
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- Youfu Zhao
- Department of Energy–Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824
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- Bonnie C. McCaig
- Department of Energy–Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824
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- Byron A. Wingerd
- Department of Entomology, Michigan State University, East Lansing, Michigan 48824
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- Jihong Wang
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109
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- Mark E. Whalon
- Department of Entomology, Michigan State University, East Lansing, Michigan 48824
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- Eran Pichersky
- Department of Biology, University of Michigan, Ann Arbor, Michigan 48109
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- Gregg A. Howe
- Department of Energy–Plant Research Laboratory, Michigan State University, East Lansing, Michigan 48824
抄録
<jats:title>Abstract</jats:title><jats:p>Jasmonic acid (JA) is a fatty acid–derived signaling molecule that regulates a broad range of plant defense responses against herbivores and some microbial pathogens. Molecular genetic studies in Arabidopsis have established that JA also performs a critical role in anther and pollen development but is not essential for other developmental aspects of the plant's life cycle. Here, we describe the phenotypic and molecular characterization of a sterile mutant of tomato (jasmonic acid–insensitive1 [jai1]) that is defective in JA signaling. Although the mutant exhibited reduced pollen viability, sterility was caused by a defect in the maternal control of seed maturation, which was associated with the loss of accumulation of JA-regulated proteinase inhibitor proteins in reproductive tissues. jai1 plants exhibited several defense-related phenotypes, including the inability to express JA-responsive genes, severely compromised resistance to two-spotted spider mites, and abnormal development of glandular trichomes. We demonstrate that these defects are caused by the loss of function of the tomato homolog of CORONATINE-INSENSITIVE1 (COI1), an F-box protein that is required for JA-signaled processes in Arabidopsis. These findings indicate that the JA/COI1 signaling pathway regulates distinct developmental processes in different plants and suggest a role for JA in the promotion of glandular trichome–based defenses.</jats:p>
収録刊行物
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- The Plant Cell
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The Plant Cell 16 (1), 126-143, 2004-01-01
Oxford University Press (OUP)
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詳細情報 詳細情報について
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- CRID
- 1364233269993038592
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- NII論文ID
- 80016434029
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- ISSN
- 1532298X
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